The above image is a light micrograph of a microscopic cyst containing Toxoplasma gondii parasites (stained red) in brain tissue.
Toxoplasmosis is a parasitic disease caused by the protozoan Toxoplasma gondii.
The parasite primarily resides in cats however humans (and other mammals) may also be infected. Contact with domesticated cats (spread in faeces) and digestion of raw meat are the main causes for infection in humans however in healthy adults the parasite will usually only lead to mild flu-like symptoms in the first weeks after exposure before the infection enters a latent phase, forming cysts in nervous and muscle tissues. The individual will then (unless immunocompromised) remain completely asymptomatic thereafter (if not so already). Once infected, a person is immune from further infection for life.
Infection is much more concerning in those with a weakened immune system, such as pregnant women and those already suffering from infection or disease (e.g. with AIDS or TB). In such cases toxoplasmosis can lead to serious illness and potential fatality. Toxoplasmosis can also be transmitted from mother to child, leading to severe complications as the infant is vulnerable and yet to develop a functioning immune system. These complications often appear at birth (or during gestation) however symptoms may not appear until a later stage in life, with greater severity than would usually be seen in an individual (more on this in another post).
The parasite can cause encephalitis (inflammation of the brain), neurologic diseases, can affect the heart, liver, inner ears, and eyes (chorioretinitis, necrotizing retinochoroiditis). Recent research has also linked toxoplasmosis to brain cancer, attention deficit hyperactivity disorder, obsessive compulsive disorder and schizophrenia.
‘In 11 of 19 scientific studies, T. gondii antibody levels were found to be significantly higher in individuals affected by first-incidence schizophrenia than in unaffected persons. Individuals with schizophrenia are also more likely to report a clinical history of toxoplasmosis than those in the general population.’
‘Recent work at the University of Leeds has found the parasite produces an enzyme with tyrosine hydroxylase and phenylalanine hydroxylase activity. This enzyme may contribute to the behavioral changes observed in toxoplasmosis by altering the production of dopamine, a neurotransmitter involved in mood, sociability, attention, motivation and sleep patterns.’
Just thought I’d give some quick updates.
-Two of my college courses are done with, now all I have is biology which I’m currently rocking an A* in.
-Off to Amurica for summer.
-Marrying the crap out of a very special man of mine.
-Then studying medicine at Manchester!
In the mean time I have posts lined up on toxoplasmosis, eyez (basic anatomy and physiology), Parkinson’s, dopamine, adipose fats and a few notes on critical periods of development in mammals. Exciting, right?
Also, feel free to ask me questions and such. For once I have a moderate amount of time on my hands. Bye bye for now.
Edit: AND I’m going stationery shopping with my dearest Owen (is this validation enough for you?).
Wolff-Parkinson-White Syndrome
This is a heart disorder occurring in approximately 0.1%-0.3% of the general population.
It is a type of pre-excitation syndrome, meaning that the ventricles depolarise (and therefore contract) prematurely.
Normally the atria and ventricles are isolated, with an electrical impulse only being able to spread from one to the other by the atrioventricular node which delays and reduces the strength of the initial impulse so ventricular contraction is regulated and does not occur too soon or too frequently.
Individuals with WPW however have an accessory pathway (as shown above) called the bundle of Kent which creates another electrical connection between the atria and ventricles, bypassing the atrioventricular node. The bundle of Kent does not delay nor reduce the strength of the initial impulse and may even increase the speed at which it is transmitted. This causes premature contraction of the ventricles and tachycardia (rapid heart rate).
When coupled with cardiac dysrhythmia (irregular heart beat), individuals with an accessory pathway have an increased risk of ventricular fibrillation. Severe tachycardia may lead to cardiogenic shock (inadequate blood circulation due to premature ventricular contraction/arrhythmia). These create a very small risk of sudden cardiac death, occurring in approximately <0.6% of WPW sufferers.
Symptoms
Many people may remain asymptomatic throughout their lives however symptoms most commonly found in WPW patients are:
Chest pain or tightness
Dizziness
Syncope (fainting)
Palpatations
Shortness of breath
Diagnosis (using an ECG when in normal sinus rhythm)
A delta wave can often be observed (manifested as a slurred upstroke beginning the QRS complex).
Short PR interval <120milliseconds
Widened QRS complex >120milliseconds
Treatment of WPW is a destruction of the abnormal electrical pathway by radiofrequency catheter ablation (an invasive procedure involving flexible catheters being threaded through the patients blood vessels to the heart and an electrical impulse being given to destroy the accessory pathway).
(Source: eviscerator)
It has been a while since I posted a photo of myself and I feel my appearance has changed somewhat. I’m making more of an effort these days.
Anyway, here’s a photo of me being all hipster and stuff.
Echocardiography
This is a type of diagnostic medical imaging that produces a sonogram/ultrasound of the heart.
There are two methods of performing the procedure, one involves a transducer being positioned on the chest of a patient (transthoracic) - similar to pregnancy scans but on the chest - and another which produces a clearer image, requiring a probe/transducer being passed into the patient’s oesophagus (transoesophageal).
Echocardiograms are used to help identify and diagnose a range of cardiac conditions, providing visual images of the shape and size of the heart, stroke volume, atrioventricular valves, anatomical and/or congenital abnormalities and tissue damage (such as that associated with ischaemia and coronary heart disease).
Biopsies
Biopsies are used for diagnostic testing and involve sampling cells or tissue for examination. The sample can then be analysed chemically or observed under a microscope to determine the presence or severity of a disease. They may also be used in therapeutic treatment by removing damaged tissue.
There are 2 types of biopsy:
Excisional - When an entire mass of tissue is removed.
Incisional - When a sample is taken without damaging the surrounding tissue (an exception being a needle aspiration biopsy).
Biopsies are often used in the treatment and diagnosis of cancer, to remove lesions and/or identify the stage and type of cancer. They may also be used in the diagnosis and monitoring of other conditions such as inflammatory bowel disease, to observe any changes that may precede malignancy and transplanted organs can be biopsied to assess whether there are any signs of rejection.
Sites often biopsied: bone marrow, gastrointestinal tract, liver, prostate, lung, breast, cervix and skin.
Osteoporosis
This is a disease that causes bone mineral density to decrease i.e. bones become porous, leading to an increased risk of fracture.
There are two main types of osteoporosis:
Primary - Affects elderly patients and is observed more so in females (with a ratio of 2:1).
Secondary - Can arise in patients of any age, affecting men and women equally. This may be due to malnutrition, medication or predisposing medical conditions.
Genetically, osteoporosis is multifactorial, meaning several genes are associated with its development - some of which are affected by environmental factors. Such modifiable environmental risk factors include: Excessive alcohol consumption, smoking, malnutrition (particularly deficiencies of vitamin D and low dietary calcium and/or phosphorus), low body weight/anorexia, sedentary lifestyle.
The diagnosis of osteoporosis can be made using conventional radiography and by measuring the bone mineral density. Investigation will then be carried out to determine potential underlying causes e.g. using blood tests to identify chemical deficiency.
Nephritis
This is an inflammation of the nephrons in the kidney. Nephrons filter and eliminate waste products from the body, regulating the concentration of substances in the blood (e.g. water and sodium).
Nephritis can be due to a number of different factors, such as infection, toxins/medication and autoimmune diseases (e.g. lupus).
If left untreated, nephritis can eventually result in renal failure. A summary of pathological symptoms and causes are as follows (see definitions at the bottom if necessary):
Oliguria and uraemia/azotaemia due to reduced glomerular blood flow (as it becomes inflamed); haematuria as tissue of glomeruli is damaged; oedma and hypertension as renal blood flow is low; proteinuria (often causes the urine to become foamy) as the absorption of the kidneys is poor and filtration is impaired.
The treatment of nephritis depends on the type and cause of the condition. The aim is to reduce inflammation, limit the damage to the kidneys and support the body until kidney function is back to normal. This may include medication (such as steroids and antibiotics), a restricted diet and in severe cases; dialysis. In adults there is a 1 in 3 chance they could develop chronic nephritic kidney disease, which would require permanent dialysis or a kidney transplant.
Definitions:
Uraemia/azotaemia - retention of waste products (retained in blood)
Haematuria - excessive presence of blood in urine
Proteinuria - excessive presence of protein in urine
Oliguria - low urinary output
Oedema - swelling/fluid retention
Hypertension - high blood pressure
Uterus didelphys
This is a congenital abnormality in which a female has two uteri, two cervices and often two vaginae. It is due to the paramesonephric ducts (also known as mullerian ducts) failing to fuse during embryogenesis. Causes for the failure to fuse are not known. It has been estimated to occur in 1 in 3000 women.
The above photograph was taken immediately prior to a laparoscopically assisted vaginal hysterectomy. This patient had delivered two children vaginally; one conceived in each uterus. This is an example of a complete uterus didelphys with two uteri, two cervices and two vaginae.
Coloured scanning electron micrograph (SEM) demonstrating the process of phagocytosis (I like to think of it as biological Pac-Man). In this example a macrophage white blood cell (purple) is engulfing Mycobacterium tuberculosis bacteria (pink).
Tuberculosis (TB)
The above image shows a coloured X-ray of pulmonary tuberculosis, caused specifically by the bacterium Mycobacterium tuberculosis.
General notes:
TB is most commonly caused by the bacterium Mycobacterium tuberculosis (MTB), which is spread by droplet infection (transmitted in saliva, usually by coughing or sneezing). MTB is highly aerobic, requiring high levels of oxygen. It affects the respiratory system, particularly damaging and destroying lung tissue.
Only about 30% of people exposed to TB will become infected. This is much more likely to occur in individuals who are immunocompromised (hence TB often presenting itself in those whom are HIV positive).
The primary infection of TB is often asymptomatic, although occasionally it may cause fever and/or a dry cough. In an individual with a healthy immune system, a localised inflammatory response will occur, forming a nodule of tissue called a tubercule (containing dead bacteria and macrophages). Typically (in about 90% of cases) the condition will resolve itself without the individual ever having known they were infected.
However MTB may survive, as alveolar macrophages are unable to digest the bacteria, allowing it to remain in a state of dormant latency and multiply silently. After a period of time, when the host’s immunity is compromised (for example, due to infection or malnourishment) the bacteria will produce active tuberculosis.
Symptoms:
When the infection presents itself in this way (referred to as miliary tuberculosis), symptoms may initially include loss of appetite, fever, productive cough and loss of energy, loss of weight/anorexia or night sweats however these are very non-specific. As the infection progresses, one may develop tuberculous pleuritis (causing chest pain, nonproductive cough and fever), increase in production of mucous and haemoptysis (coughing up blood).
As the infection spreads it may lead to symptoms such as abdominal pain, painful urination, sterility and brain damage (depending on which areas are affected and to what extent).
Treatment and prevention:
If left untreated, TB will eventually cause death. This may be because of hypoxia (due to severe lung damage) or organ failure (due to malnutrition). Also, as TB disarms a critical part of the immune system, it makes patients much more susceptible to opportunistic infections (such as pneumonia) therefore patients are often treated with antibiotic medication outside of a hospital environment. Vaccines are commonly administered as a form of prevention and are effective against severe forms of paediatric TB however adult pulmonary TB is still prevalent (there are currently more TB cases worldwide than ever before).
Diagnosis:
An X-ray may indicate the presence of TB however other infections appear similar so cultures must be taken to confirm the diagnosis.
Human immunodeficiency virus (HIV)
The above image is a coloured SEM of HIV (yellow) budding from host cells (red).
General notes:
HIV is part of the retrovirus family, which causes AIDS (acquired immunodeficiency syndrome), resulting in progressive failure of the immune system. It can be transferred in blood, semen, vaginal fluid, pre-ejaculate and breast milk. HIV has a long latency/incubation period.
HIV infects vital cells in the immune system, particularly CD4+T helper cells (a type of white blood cell called lymphocytes). The infection of the HIV virus causes the number of T-helper cells to decline, making the body more susceptible to opportunistic infections (such as tuberculosis). It is these secondary infections (or malignancies) that will eventually cause death.
A2 level notes on how HIV works:
The HIV envelope has surface proteins, which recognise and bind to surface proteins on T-helper cells. HIV then infects the T helper cell and viral mRNA enters the host.
Note: Reverse transcriptase found in the virion is an enzyme that makes DNA from mRNA. This DNA codes for viral coat proteins and recognition proteins. DNA made by reverse transcriptase can be called complementary DNA (cDNA) as it is complementary to mRNA.
cDNA passes from the cytoplasm of the T-helper cell into the nucleus (integrase protein helps cDNA pass through the nuclear pore and inserts DNA into the host cell chromosome).
Viral cDNA is transcribed to viral mRNA. Viral mRNA is then translated to protein capsomeres. Virions self-assemble and cell lyses as virions exit the host cell (exocytosis).
A2 level notes on the course of a HIV/AIDS infection:
Stage 1: Acute HIV syndrome. Between 3-12 weeks post-infection, HIV antibodies appear in the blood (now HIV positive). Symptoms experienced during this time may include fever, headache, dizziness and swollen glands.
Stage 2: Asymptomatic/chronic stage. All symptoms disappear once the infection has been established. Virus is now latent. The duration of this stage depends on health, immunity, genetics and access to medication. During this stage the virus replicates, infecting T helper cells but being restrained by T killer cells. Towards the end of this stage the immune system becomes overwhelmed and secondary infections begin to develop.
Stage 3: Symptomatic stage. Eventually the viral load becomes so great that the whole immune system starts to fail. The normal T helper cell count falls from 500 to 200 per mm3 of blood. Symptoms now suffered include weight loss, fatigue, diarrhoea, night sweats and low-grade infections such as candidiasis (thrush). This stage rapidly progresses to the final stage.
Stage 4: Advanced AIDS. T helper cell numbers continue to fall. Symptoms include severe weight loss, dementia (as brain cells become infected), cancers (e.g. Kaposi’s sarcoma) and serious infections (e.g. tuberculosis (note: HIV is the main cause for an increase in TB infection) and cryptococcal meningitis). The final stage of advanced AIDS is always death.
Rocking my oversized lab coat at Keele university (on a genetics trip).
More personal stuff/bragging:
Got an A* in my bio exam annnnd it’s only 29 days until my boyfriend gets here!
Also, UEA have sent me the next step of the medical application (a questionnaire thingy).
Let the January exam prep begin!
